Allergic dermatitis can be caused from contact with hydrophobic toxins found in plants, insects, and animals.
Urushiol is a commonly encountered hydrophobic toxin in the exudate of plants such as poison ivy, poison oak, poison sumac, and related plants in the Anacardiaceae group. Some experts estimate there are up to 55 million cases of urushiol-induced contact dermatitis annually in the United States. When adequately exposed to urushiol containing plants, it has been estimated that about 85 percent of all people will develop an allergic reaction.
Urushiols are mixtures of catechols with long, hydrophobic, carbon (alkyl) side chains at the three position of the catechol ring. Poison ivy contains predominately 3-n-pentadececylcatechols (C-15) and poison oak contains predominantly 3-n-heptaecylcatechols (C-17).
After exposure, urushiol binds to the skin causing a rash to develop within two days. The rash peaks in five days and can take two or more weeks to heal. Redness, swelling, blisters, and severe itching are typical urushiol-induced dermatologic reactions. The rash appears to spread when it breaks out in new areas. Urushiol is absorbed more slowly where the skin is thicker, such as on forearms, legs, and the body's trunk. Urushiol can be transferred by fingernails or animal fur and can remain on clothing, shoes, and tools for up to five years in moist climates.
The red imported fire ant (Solenopsis invicta) has invaded over 300 million acres in the United States. The red imported fire ant is aggressive and has a powerful sting that has caused the deaths of at least 80 people, injury to tens of thousands of people annually, and injury and death of wildlife, livestock, and pets.
Fire ant venom differs from other insect venoms, which are mostly proteinaceous solutions. Fire ant venom is a hydrophobic toxin that includes isosolenopsin A and some minor proteins. Isosolenopsin A is a water insoluble dialkyl piperdine alkaloid. The substitutions of the piperdine ring are long chain aliphatic members. Isosolenopsin A can induce the release of histamine and other vasoactive amines from mast cells, resulting in a sterile pustule at the sting site. The toxicity of isosolenopsin A is believed to cause the pustules to form. Large, local reactions can also cause edematous tissue compression that can compromise the vascular supply to the effected area.
Urushiol and isosolenopsin A are mixtures of long hydrophobic-chained molecules that readily oxidize and react with proteins. The toxins can exist in both native and oxidized states on dermal layers.
Treatment of oleoresin-induced allergic dermatitis has historically involved washing the exposed area with soap and water and/or applying an astringent such as alcohol or witch hazel. People tend to fail at fully removing the oleoresin toxin before it has bound to the dermal proteins of the skin.
Other treatments of oleoresin-induced allergic dermatitis consist of steroids, anti-inflammatory, and antihistamine compounds that temporarily treat the symptoms of the response but do nothing to remove the toxin, which initiated the response.
U.S. Pat. No. 7,008,963, U.S. Pat. No. 6,423,746; and EP Patent App. 1762227A2 disclose several compositions with an abrasive factor to remove oleoresins from the exposed areas. However, these compositions contain high levels of surfactants capable of chemically-induced sensitivity and dermatitis themselves.
Other attempts for toxin removal can be seen in U.S. Pat. Nos. 5,686,074 and 5,620,527, but both patents utilize agents that can cause dermatitis themselves.
The method described herein advantageously provides an improved method for treating allergic dermatitis caused by exposure to naturally-occurring hydrophobic toxins.